If children indeed employ a lower proportion of type-II motor units during exercise, they should be expected to demonstrate lower carbohydrate and higher fat metabolism. Riddell et al. (79) found that during graded exercise, fat oxidation rates peaked at
Phase II of the pulmonary VO2 kinetics, following exercise onset, is thought of as closely reflecting the oxygen uptake kinetics of the working muscles (9). At any relative exercise intensity, faster phase-II kinetics would be expected in individuals with higher relative aerobic power (maxVO2) (74), muscle oxidative capacity, or type-I muscle-fiber composition (8). If children do not use type-II motor units to the same extent as adults, their muscles would be characterized by higher functional composition of type-I muscle fibers and would be expected to have faster muscle VO2 kinetics and consequently demonstrate faster phase-II pulmonary VO2 kinetics. Indeed, in comparison with adults or adolescents of comparable or even somewhat superior aerobic power, children have been repeatedly shown to attain a given percentage of the ultimate VO2 response faster than adults (38,86,95).
Thus, children’s lower lactate response, faster PCr and VO2 kinetics and greater reliance on fat oxidation provide equivocal support to the differential metabolic profile and differential motor-unit activation hypotheses, as well as to differential Meetville muscle composition ( Table 1 ).
Following resistance training, children have been shown to proportionately improve their strength to an extent similar to that observed in adults (80,81). However, while strength gains in adults are typically closely tied to muscular hypertrophy, only a limited hypertrophic response has been found in adolescents (64), and none could generally be shown in prepubertal children (see (12,81) for review).
While training-induced hypertrophy in prepubertal children cannot be dismissed (66,93), it is generally agreed that, when present, it is exceedingly smaller than that observed in adults and far too small to account for the observed strength gains (12). Thus, training-induced strength gains in prepubertal children must be due to increased muscle activation (12,19,36,82). Indeed, Ramsay et al. (75) found a 13–17% trend toward increased motor-unit activation in prepubertal boys, following 20 weeks of resistance training, while Ozmun et al. (71) found a 16.8% increase in integrated EMG activity following 8 weeks of training.
This difference in the mechanism of training-induced strength-gain between children and adults is nicely supported by the findings of Faigenbaum et al. (33). The authors examined strength gains following 8 weeks of low-repetition, heavy-resistance vs. high-repetition, moderate-resistance training protocols in prepubertal children. Both training protocols resulted in increased strength. However, while in adults, greater strength gains would be expected in the low-repetition, heavy-resistance protocol, the children’s strength gains were similar or greater in the high-repetition, moderate-resistance protocol. This appears to suggest that, in children, the higher resistance could not significantly access the higher-threshold motor units, rendering that form of training less efficient than the lower-resistance, higher-repetition protocol that simply provided a more extended training stimulus.
Adults also exhibit neuro-motor adaptations to resistance training, but these are largely confined to the first few weeks of training (43). Muscle hypertrophy, likely dependent on androgen levels, typically accounts for most of the strength gains beyond the initial weeks (43). It could be expected that due to their low androgen levels, children would be limited in their training-induced gains. However, the fact that children exhibit proportionately similar or even greater (81) strength gains than adults, strongly suggests that they have considerably larger untapped motor-unit recruitment and utilization capacity. Thus, children’s nonhypertrophic but adult-comparable strength gains constitute very strong evidence in support of the differential motor-unit activation hypothesis, or a general activation deficit, and cannot be explained by differential muscle composition.